Can Immunosuppression Slow the Progression of Primary Glomerulonephritis?

IgA nephropathy (IgAN) is the most common primary glomerulonephritis in the world. It was first described in 1968 by Jean Berger and Nicole Hinglais as the presence of intercapillary deposits of IgA. Despite this simple description, patients with IgAN may present very broad clinical features ranging from the isolated presence of IgA in the mesangium without clinical or biological manifestations to rapidly progressive kidney failure. These features are associated with a variety of histological lesions, from the discrete thickening of the mesangial matrix to diffuse cell proliferation. Immunofluorescence on IgAN kidney specimens shows the isolated presence of IgA or its inconsistent association with IgG and complement components. This clinical heterogeneity of IgAN clearly echoes its complex and multifactorial pathophysiology in humans, inviting further analyses of its various aspects through the use of experimental models. Small-animal models of IgAN provide the most pertinent strategies for studying the multifactorial aspects of IgAN pathogenesis and progression. Although only primates have the IgA1 subclass, several murine models have been developed in which various aspects of immune responses are deregulated and which are useful in the understanding of IgAN physiopathology as well as in the assessment of IgAN therapeutic approaches. In this manuscript, we review all murine IgAN models developed since 1968 and discuss their remarkable contribution to understanding the disease.

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T helper (Th)-cytokines in the urine of patients with primary glomerulonephritis treated with immunosuppressive drugs: Can they predict outcome?

Cytokine ◽

10.1016/j.cyto.2015.08.002 ◽

2015 ◽

Vol 76 (2) ◽

pp. 260-269 ◽

Cited By ~ 12

Author(s):

Dimitra Kalavrizioti ◽

Miltiadis Gerolymos ◽

Maria Rodi ◽

Pantelitsa Kalliakmani ◽

Simela Provatopoulou ◽

...

Keyword(s):

Immunosuppressive Drugs ◽

T Helper ◽

Primary Glomerulonephritis

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Tu-P7:104 Preclinical cardiovascular abnormalities and thrombotic risk in patients with primary glomerulonephritis with mild or no impairment of renal function

Atherosclerosis Supplements ◽

10.1016/s1567-5688(06)80810-x ◽

2006 ◽

Vol 7 (3) ◽

pp. 207

Author(s):

V. Palmieri ◽

P. Esposito ◽

S. Martino ◽

C. Russo ◽

P. Migliaresi ◽

...

Keyword(s):

Renal Function ◽

Thrombotic Risk ◽

Primary Glomerulonephritis ◽

Cardiovascular Abnormalities

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Crosstalk between proteinuria, plasma oxalic acid and inflammation in glomerulonephritis patients: an exploratory study

Ukrainian Journal of Nephrology and Dialysis ◽

10.31450/ukrjnd.3(71).2021.03 ◽

2021 ◽

pp. 19-27

Author(s):

Natalia Stepanova ◽

Lyudmyla Snisar ◽

Larysa Lebid ◽

Victoria Driianska

Keyword(s):

Risk Factor ◽

Glomerular Filtration Rate ◽

Cardiovascular Risk ◽

Oxalic Acid ◽

Healthy Volunteers ◽

Acid Concentration ◽

Filtration Rate ◽

Primary Glomerulonephritis ◽

Nephrotic Proteinuria ◽

Oxalic Acid Concentration

Abstract. In the present exploratory cross-sectional cohort study, we evaluated whether plasma and urine oxalate concentrations in patients with primary glomerulonephritis depend not only on the glomerular filtration rate but also on the proteinuria level and influence the inflammatory response. Methods. We enrolled 100 participants, including 76 patients with glomerulonephritis having chronic kidney disease stage (CKD) 1–3b (69.7% of them with nephrotic syndrome) and 24 healthy volunteers. We excluded patients with diabetes, cardiovascular disease and those with glomerulonephritis with an estimated GFR (eGFR) < 30 mL/min/1.73 m2. In addition to routine hematological and biochemical tests, plasma oxalate concentration, urinary oxalate excretion, and serum interleukin (IL)-6 and monocyte chemoattractant protein-1 (MCP-1) levels were assessed in all study participants. Results. We observed that plasma oxalic acid concentration was significantly higher in patients with glomerulonephritis (19.0 [5.9–45.2] µmol/L) than in healthy volunteers (5.5 [3.8–7.3] µmol/L, p < 0.0001). Moreover, nephrotic proteinuria was significantly associated with plasma oxalic acid elevation independent of the patients’ age, sex, glomerular filtration rate, and body mass index (odds ratio = 1.42, 95% confidence interval = 1.13–1.77, p = 0.002). In turn, the increased plasma oxalic acid concentration was associated with high levels of serum IL-6 and MCP-1, which may be cardiovascular risk factors in patients with primary glomerulonephritis. Conclusions. Nephrotic proteinuria was significantly associated with the elevation of plasma oxalic acid concentration and hyperoxaluria in glomerulonephritis patients with CKD stages 1–3b. Plasma oxalate at least partly promotes inflammation, which may be a cardiovascular risk factor in patients with glomerulonephritis in the early stages of CKD. Future studies should recruit at least 156 participants to confirm our preliminary results, validate nephrotic proteinuria as a risk factor for oxalate metabolism violation or determine the role of impaired oxalate homeostasis in clinical outcomes in patients with glomerulonephritis.

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